HIF-1α modulates β-catenin pathway to enhance the survival and angiogenesis of PBMSCs under hypoxia environment

Figure 8 Hypoxia-inducible factor-1α/β-catenin signaling enhances angiogenesis and inhibits apoptosis of peripheral blood mesenchymal stem cells in infarcted hearts. The experiment was categorized into 6 groups, including sham, myocardial infarction, hypoxia-inducible factor-1α (HIF-1α) overexpression, β-catenin overexpression, HIF-1α knockdown plus β-catenin overexpression, or HIF-1α overexpression plus β-catenin knockdown-transfected peripheral blood mesenchymal stem cell groups. A: The collagen density of each group was determined by trichrome staining. Hematoxylin and eosin staining revealed varying degrees of fibrocyte infiltration and inflammation (scale bar = 50 μm); B and C: Representative immunoblots and analysis of the protein expression of hypoxia-inducible factor-1α, β-catenin, basic fibroblast growth factor, vascular endothelial growth factor, survivin, Bax, Bcl2, and cleaved caspase 3. All graphical data are presented as the means ± SEMs. ^aP < 0.05; ^bP < 0.01; ^cP < 0.001. n = 5 in each group. H&E: Hematoxylin and eosin; MI: Myocardial infarction; oeHIF-1α: Hypoxia-inducible factor-1α overexpression; shHIF-1α: Hypoxia-inducible factor-1α knockdown; oeβ-catenin: Β-catenin overexpression; shβ-catenin: Β-catenin knockdown; HIF-1α: Hypoxia-inducible factor-1α; VEGF: Vascular endothelial growth factor; bFGF: Basic fibroblast growth factor.